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Associations of serotonergic genes with poststroke emotional incontinence
Author(s) -
Kim JaeMin,
Stewart Robert,
Kang HeeJu,
Bae KyungYeol,
Kim SungWan,
Shin IlSeon,
Kim JoonTae,
Park ManSeok,
Cho KiHyun,
Yoon JinSang
Publication year - 2012
Publication title -
international journal of geriatric psychiatry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.28
H-Index - 129
eISSN - 1099-1166
pISSN - 0885-6230
DOI - 10.1002/gps.2787
Subject(s) - serotonergic , serotonin transporter , allele , depression (economics) , genotype , stroke (engine) , 5 httlpr , psychology , logistic regression , gene , serotonin , population , genetics , medicine , biology , neuroscience , receptor , mechanical engineering , macroeconomics , environmental health , engineering , economics
Objectives Poststroke emotional incontinence (PSEI) has been associated with serotonergic dysfunction. Polymorphisms of serotonin transporter (5‐HTT) and serotonin 2a receptor (5‐HTR2a) genes may regulate serotonergic signaling at brain synapses, and this study was to investigate associations with PSEI in an East Asian population. Methods In 276 stroke cases, PSEI was diagnosed by Kim's criteria. Covariates included age, gender, education, history of depression or stroke, current depression, and stroke severity and location. Genotypes were ascertained for 5‐HTT gene‐linked promoter region (5‐HTTLPR), serotonin transporter intron 2 variable number tandem repeat, 5‐HTR2a 1438A/G, and 5‐HTR2a 102 T/C. Associations with PSEI were estimated by using logistic regression models, and gene–gene interactions were investigated by using the generalized multifactor dimensionality reduction method. Results PSEI was present in 37 (13.4%) patients. The 5‐HTT gene‐linked promoter region s / s genotype was independently associated with PSEI. No associations with STin2 VNTR and 5‐HTR2a genes were found, and no significant gene–gene interactions were identified. Conclusions Stroke patients with 5‐HTTLPR s allele had higher susceptibility to PSEI, which underlines the potential role of serotonergic pathways in its etiology. Copyright © 2011 John Wiley & Sons, Ltd.